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Imidazoline receptors of the paraventricular nucleus on the pressor response induced by stimulation of the subfornical organ
Institution:1. Department of Cardiology, Zhongshan Hospital Fudan University, Shanghai 210032, China;2. Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY 82071, USA;3. The Second Department of Cardiology, The Third Hospital of Nanchang, Nanchang, Jiangxi 330009, China;4. Department of Physiology, Eastern Virginia School of Medicine, Norfolk, VA, USA;5. Department of Obstetrics and Gynecology, Daping Hospital, Third Military Medical University, Chongqing 400038, China
Abstract:In the present experiments we investigated a possible involvement of imidazoline receptors of the paraventricular nucleus (PVN) of the hypothalamus on the pressor effects of the angiotensin II (ANG II) injected into the subfornical organ (SFO), in male Holtzman rats (250–300 g) with a cannula implanted into the third ventricle (3rdV), PVN and SFO. At first we tested the participation of α2 and imidazoline agonist and antagonist compounds on the pressor effect of ANG II injected into the 3rdV. Based on the results we may conclude that clonidine associated with rilmenidine was able to block the hypertensive response to ANG II. The ANG II (20 pmol) injected into SFO induced a robust increase in blood pressure (37 ± 2 mmHg). Isotonic saline (0.15 M) NaCl did not produce any change in blood pressure (5 ± 2 mmHg). The injection of rilmenidine (30 μg/kg/1 μL), an imidazoline agonist agent injected into PVN before ANG II injection into SFO, blocked the pressor effect of ANG II (5 ± 2 mmHg). Also, the injection of idazoxan (60 μg/kg/μL) before rilmenidine blocked the inhibitory effect of rilmenidine on blood pressure (39 ± 4 mmHg). The injection of clonidine (20 nmol/μL) prior to ANG II into the 3rdV produced a decreased in arterial blood pressure (37 ± 2 mmHg) to (15 ± 4 mmHg). The injection of yohimbine (80 nmol/μL) prior to clonidine blocked the effect of clonidine on the effect of ANG II (27 ± 2 mmHg). The injection of rilmenidine prior to ANG II also induced a decrease in arterial blood pressure (10 ± 3 mmHg). The injection of idazoxan prior to rilmenidine also blocked the inhibitory effect of rilmenidine (24 ± 3 mmHg). In summary, the present study demonstrated that rilmenidine decreases the hypertensive effect of ANG II, with more potency than clonidine, even when injected into 3rdV or PVN. This study established that the PVN interacts with SFO by imidazoline receptors in order to control the arterial blood pressure.
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